In Article <4481lc$cru at nntp.ucs.ubc.ca> ""Steven H. Pullen" <shpullen at unixg.ubc.ca>" says:
> As I understand, somaclonal variation is a major obstacle in regererating
> Arabidopsis (re: after generating insertional mutations via T-DNA). I am
> currently taking my first course in plant genetics and I cannot find
> a very good definition of what exactly somaclonal variation is and how
> its arises during tissue culturing. I'm afraid this might be a reletively
> easy question but I've exhausted all of my (limited) resources. Any help
> would be greatly approciated. Thanks in advance.
>.
Somaclonal variation: Somatic mutations which are clonaly propagated.
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Mutations happen all the time. Every scheme for isolating insertion mutants
(transposon, T-DNA, etc) is plagued by random mutations. For more info about
somaclonal mutation, try looking up some of the early work by Evans and
Sharp. In a nutshell, the frequency of somatic mutation in tissue culture
can be increased or decreased by certain practices. As I recall, higher auxin
levels and longer time spent in the de-differentiated state both tend to
increase mutation rates. I am not aware of any evidence that the rate of
somatic mutation in a minimised protocol is any different than the normal
rate. In personal discussions with Dr. Evans, he suggested that the rate of
mutation in his minimised system is not statistically different from the non-
tissue culture rate of mutation (or so it appeared to him in preliminary
observations at that time). At that time he was focussing most of his effort
on maximising mutation rates to increase variation for selection in breeding
programs. Bottom line, minimise exposure of your plants to known mutagens.
Random mutations are likely to be an issue in any tagging experiment, find
a way to weed them out quickly. Good luck.
.
Leonard N. Bloksberg
bloksber at pilot.msu.edu
.
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